Experimental Evidence of Remodeling after Angioplasty

Abstract

Despite fifteen years of intensive research, restenosis of arteries occurring after angioplasty remains unpredictable and unpreventable. Analysis of the failure to inhibit restenosis raises questions about the pathophysiology classically used to identify restenosis, i.e., smooth muscle cell proliferation (1–4). It is well established that balloon angioplasty commonly induces a neointimal formation with smooth muscle migration from the media, and proliferation, followed by secretion of extracellular matrix (4, 5). Since restenosis often follows angioplasty, it has therefore been attributed to the occurrence of neointimal hyperplasia, the so-called tumoral concept (3, 5). Experimental models designed to reproduce neointimal proliferation were used to test various strategies targeted against smooth muscle cell proliferation (6–8). However, the success obtained in animal models was not reproduced in humans (9). The need to analyze this failure led to reevaluation of the value of experimental models and also questioned the pathophysiology of restenosis itself on a de novo basis, i.e., the tumoral concept, and to “discover” the remodeling concept which in fact existed before restenosis.